Objective:To investigate the improvement effects and mechanism of matrine(Mat)on inflammation and pulmo-nary fibrosis in rats with chronic obstructive pulmonary disease(COPD)based on the transforming growth factor-β1(TGF-β1)/signal transduction protein Smad3 pathway.Methods:The COPD model rats were established by the method of smoking combined with lipo-polysaccharide(LPS).The rats were grouped into COPD group,Mat group(100 mg/kg)and Mat+TGF-β1 group(100 mg/kg Mat+1.25 μg/kg TGF-β1),in addition,with 15 rats in each group.Another 15 randomly selected rats were set as a control group before modeling.Lung function analyzer was applied to detect the lung function of rats;HE staining was applied to observe the pathological changes of lung tissue in rats;the contents of TNF-α,IL-1β,TGF-β1 in the supernatant of alveolar lavage fluid(BALF)were detect-ed by ELISA;TUNEL staining was applied to observe apoptosis in lung tissue;immunohistochemistry was applied to detect the expres-sions of caspase-3 and matrix metalloproteinase-9(MMP-9)proteins in lung tissue;Western blot was applied to detect the expression of TGF/Smad3 pathway related proteins.Results:Compared with the control group,there were obvious inflammatory cell infiltration and cell exfoliation in the lung tissue of COPD rats,FVC,FEV0.1/FVC,FEV0.3/FVC obviously decreased(P<0.05);the levels of TNF-α,IL-1β,TGF-β1,the number of apoptotic cells,the expressions of caspase-3,MMP-9,TGF-β1,p-Smad3,Fibronectin,Col-lagen Ⅰ and α-SMA obviously increased(P<0.05);compared with COPD group,the pathological damage of lung tissue in Mat group was obviously improved,while FVC,FEV0.1/FVC and FEV0.3/FVC obviously increased(P<0.05);the levels of TNF-α,IL-1β,TGF-β1,the number of apoptotic cells,the expressions of caspase-3,MMP-9,TGF-β1,p-Smad3,Fibronectin,Collagen Ⅰ and α-SMA obviously increased(P<0.05);compared with Mat group,Mat+TGF-β1 group obviously reversed the improvement effect of Mat on COPD rats.Conclusion:Mat can improve pulmonary inflammation and fibrosis in COPD rats,which may be related to inhibiting the activation of TGF-β1/Smad3 pathway.

Objective:To investigate the improvement effects and mechanism of matrine(Mat)on inflammation and pulmo-nary fibrosis in rats with chronic obstructive pulmonary disease(COPD)based on the transforming growth factor-β1(TGF-β1)/signal transduction protein Smad3 pathway.Methods:The COPD model rats were established by the method of smoking combined with lipo-polysaccharide(LPS).The rats were grouped into COPD group,Mat group(100 mg/kg)and Mat+TGF-β1 group(100 mg/kg Mat+1.25 μg/kg TGF-β1),in addition,with 15 rats in each group.Another 15 randomly selected rats were set as a control group before modeling.Lung function analyzer was applied to detect the lung function of rats;HE staining was applied to observe the pathological changes of lung tissue in rats;the contents of TNF-α,IL-1β,TGF-β1 in the supernatant of alveolar lavage fluid(BALF)were detect-ed by ELISA;TUNEL staining was applied to observe apoptosis in lung tissue;immunohistochemistry was applied to detect the expres-sions of caspase-3 and matrix metalloproteinase-9(MMP-9)proteins in lung tissue;Western blot was applied to detect the expression of TGF/Smad3 pathway related proteins.Results:Compared with the control group,there were obvious inflammatory cell infiltration and cell exfoliation in the lung tissue of COPD rats,FVC,FEV0.1/FVC,FEV0.3/FVC obviously decreased(P<0.05);the levels of TNF-α,IL-1β,TGF-β1,the number of apoptotic cells,the expressions of caspase-3,MMP-9,TGF-β1,p-Smad3,Fibronectin,Col-lagen Ⅰ and α-SMA obviously increased(P<0.05);compared with COPD group,the pathological damage of lung tissue in Mat group was obviously improved,while FVC,FEV0.1/FVC and FEV0.3/FVC obviously increased(P<0.05);the levels of TNF-α,IL-1β,TGF-β1,the number of apoptotic cells,the expressions of caspase-3,MMP-9,TGF-β1,p-Smad3,Fibronectin,Collagen Ⅰ and α-SMA obviously increased(P<0.05);compared with Mat group,Mat+TGF-β1 group obviously reversed the improvement effect of Mat on COPD rats.Conclusion:Mat can improve pulmonary inflammation and fibrosis in COPD rats,which may be related to inhibiting the activation of TGF-β1/Smad3 pathway.

The imbalance of microbiota is related to various diseases in the human body,and the gut,as the largest microbial habitat in the human body,is closely related to the oral microbial environment.The oral microbiota can migrate to the intestinal mucosa with the digestive system.At the same time,microbial transmission from the gut to the mouth can also occur through interpersonal and com-munity transmission.Microbial transmission between the mouth and intestines can shape or reshape the microbial ecosystem in the two habitats,ultimately regulating the pathogenesis of the disease.The dysbiosis of the oral-gut microbiota axis can have a significant impact on related diseases such as respiratory diseases.This article reviews the research status of the relationship between oral-gut microbes and respiratory diseases.